27 Month delay in nyala case

10.İİİ On 28 June 1986 Mr Jeffrey examined tissue
sections taken from the brain of a nyala which had
been kept at Marwell Zoo.(S Jeffrey para 6; YB86/7.8/1.1 ) This examination, and
subsequent consideration of the report, are described
in the CVL DFA.

51.İİİ On 10 June 1987 Mr Bradley sent a BSE update to Dr Watson. It discussed, amongst other
things, the nyala case and subsequent paper, the work of Mr Wilesmith, the upcoming BCVA meeting
and the work of Dr Kimberlin.(YB 87/6.10/1.1 )

63.İİİ On 22 June 1987 Mr Bradley sent a memo to Mr Wells detailing actions taken to date. It noted
that publication has been discussed with the CVO and halted and that there were now at least 9
suspect herds and a case in a gemsbok at Marwell.(YB 87/6.22/2.1 )

74.İİİ On 1 July 1987, Mr Bradley wrote to Mr Jeffrey to tell him that his article on spongiform
encephalopathy in a nyala was not authorised for publication, and that while he made comparisons with scrapie, the CVO was unlikely to give his approval.(YB87/6.29/3.1; YB87/7.1/2.1; YB87/7.1/3.1-3.10 ) This is further discussed in the CVL DFA.

153.İİİ On 11 December 1987, Mr Jeffrey's paper on the nyala was submitted for publication in the
journal Veterinary Pathology. The paper had first been drafted the paper in autumn 1986. (S 64 Jeffrey para 10)
The title of the paper was changed from 'A scrapie-like disorder in a nyala' to 'A spongiform
encephalopathy in a nyala.' Other references to scrapie were also amended.( S Jeffrey para 10; S 65 Wells para 55; YB87/11.11/2.1; YB87/11.17/3.1; YB87/11.23/2.1. )

Spongiform encephalopathy in a nyala (Tragelaphus angasi).

166. In January 1988, Mr Wilesmith was informed of the June 1987 case of SE in the gemsbok. He
discovered from the Winchester VIC that both the nyala and the gemsbok had received rations
containing MBM and this provided further support for his hypothesis.( S Wilesmith para. 37)

More delays for"veterinary political reasons"

28.İİİİ On 28 June 1986 Dr Jeffrey examined tissue sections taken from the brain of a
nyala which had been kept at Marwell Zoo. (S Jeffrey para 6; YB86/7.8/1.1 ) The nyala had shown unusual nervous
symptoms two weeks prior to being put down on welfare grounds. These symptoms included
'weaving with the head and neck, holding the head on its side and frequent nibbling near the
tailbone.'(YB86/6.23/1.1 ) The sections were originally necropsied by Mr Geoff Holmes at the Winchester
VIC.(YB86/5.29/1.1; YB86/6.18/1.1 ) The nyala (tragelaphus angasi) is not an antelope but belongs to the same family
(species group) as cattle.

29.İİİİ Dr Jeffrey observed that the brain showed taxonomic lesions of spongiform
encephalopathy and that the similarity of the lesions to natural sheep scrapie was striking,
and indeed he thought that in comparison to natural sheep scrapie the lesions were
particularly florid.(YB86/7.2/1.1; S Jeffrey para 9 ) The sites (neuroanatomical location) and cellular location (grey
matter neuropil and neuronal cytoplasmic vacuolation) were distinctive and characteristic of
the TSEs. Dr Jeffrey sent a slide of the nyala brain to Dr Richard Kimberlin at the NPU in the
latter quarter of 1986 who 'vividly recollect[ed] seeing the results down the microscope
because the pathology was so striking'.(YB 98/11.18/1.1 )

30.İİİİ Following a field visit to Marwell Zoo on 21 July 1986,(YB86/7.24/1.1 ) a report was compiled
by Mr Holmes at Winchester VIC and a scientific paper prepared for publication in a
journal.(S Jeffrey para 10 ) Dr Jeffrey conferred with Mr Wells, his line manager at the CVL, in the
preparation of the paper.(S Jeffrey para 9; S Wells 1st para 55 ) Dr Jeffrey was not sure of the exact date he submitted the paper
to the Animal Health and Veterinary Group (AHVG) for publication but said it was some time in
Autumn 1986.(S Jeffrey para 10; YB86/11.00/1.1 ) Dr Jeffrey did not form any conclusions about the origins of the disease in
this animal, but he discussed the case with the CVL Epidemiology Department, and they agreed
to keep a 'watching brief' on the situation.(S Wilesmith para 11)

89. On 17 June 1987 the Annual Report of the CVO for 1986 was published, having been
submitted for publication on 1 June 1987.( M24 Tab 2 at 69 ) The Report described the discovery of a
'Scrapie-like disease in a captive nyala' and noted that 'Transmissible spongiform
encephalopathies have been reported in man, sheep and goats (scrapie), mule deer and mink.'

91. On 19 June 1987 Mr Bradley sent Dr Watson a BSE Update. Amongst other things it was
noted:(YB 87/6.19/3.1-3.2 )

"The final draft Vet Rec paper has been prepared and
submitted for authority to publish. This has been rejected by
CVO whilst scrapie is mentioned. For this and other reasons
the paper is temporarily withdrawn until further
information is available"

92. On 19 June 1987 Dr S.H. Done diagnosed spongiform encephalopathy in a gemsbok from
Marwell Park.(YB87/6.19/3.2; YB876.8/3.1; YB87/6.10/3.1; YB87/6.25/1.1 ) This was the zoo was from which the SE-infected nyala had come. While
the nyala was from the same species group as cattle, the gemsbok is an African antelope.

100. On 1 July 1987 Mr Bradley wrote to Dr Jeffrey to tell him that his article on
spongiform encephalopathy in a nyala was not authorised for publication, and that while he
made comparisons with scrapie, the CVO was unlikely to give his approval.(YB87/7.1/3.2; YB87/6.29/3.1; YB87/7.1/2.1 ) The initial
title of the paper was 'Scrapie-like disorder in a nyala'.( S Jeffrey para 12 ) At the request of Tolworth, the
title of the paper was eventually changed to 'Spongiform encephalopathy in a nyala'.( YB87/11.00/1.1 )
Because of the original references to the scrapie-like nature of the disorder the paper was
delayed for publication and was not published until September 1988.( J/VP/25/398 ) Dr Jeffrey told the
BSE Inquiry that he resisted the move to alter his paper because it 'would have been negligent
to try and publish that without a reference to scrapie'.(T25 at 32 )

157. On 17 November 1987 Mr Bradley minuted Dr Jeffrey noting that the title to his nyala paper
was likely to be unacceptable to "senior management" for "veterinary political reasons". He also
recommended that where comparisons were made with scrapie the emphasis ought to be
altered.(YB 87/11.17/1.1 )

433. On 23 October 1989 Dr Watson told Mr Wells that the CVL were to supply material from the
kudu and nyala to the NPU for transmission to mice. Dr Watson said this was an important
transmission experiment designed to establish the relationship between the disease in zoo animals and
cattle.(S Watson 1st para 134 ) Mr Bradley provided Dr Watson with a list of tissues that were to be sent to the NPU on
24 November 1989.(YB89/10.24/4.1 )

Sordid events at Central Veterinary Laboratory

19.İİİİ On 24 January 1990 Mr Bradley sent to Dr Watson a summary of the main points of a meeting held with the Minister the same day.(20) The minute noted:

"The Minister played Devil's advocate in relation to: -
1. Potential for scrapie to be as much a potential danger to man as BSE was perceived to be...
2. Was concerned about the risk to pigs via MBM & thus to man..
3. Was advised by the CVO of possible concern in horses
4. Had serious concern about feeding animal protein to herbivores at all - strong public feelingä.
5. MBM exports unethical. All should be labelled & a letter should be sent to all countries to which MBM was exported should be sent."

28.İBy 12 February 1990 the nyala and kudu
tissues and the placenta had been inoculated into
mice at the NPU.(33) After his investigations into the
alimentary tract, ... Mr Bradley said in a
minute dated 12 February 1990 that:(36) "It is very clear that it is important to initiate
studies now in a much wider range of tissues
and in multiple specimens than can be
accommodated in the annual quota of 30 for
the next two years."
Mr Bradley attached a table showing the progress of
infectivity studies:

46. On 28 June 1990 Mr Bradley informed Mr Wells that a survey of hounds was to
commence.(68) The hound survey arose because the Tyrrell Committee had recognised that
domestic pets might prove susceptible to the unconventional agent of BSE and recommended
monitoring the health of animals fed offal, carcases or meat and bone meal.(M11a Tab 8 )

47. A total of 444 hound brains of mixed breeds from 101 kennels across the United Kingdom were collected and examined. Histopathological changes consistent with a florid
spongiform encephalopathy similar to that reported in cats was not observed. However, the report
of the survey identified serious flaws in the survey's design. Mr Wells said in a minute to Mr Bradley
in October 1991 that 'the survey as designed has little to offer scientifically'.(YB91/10.17/1.1)

54. On 20 August 1990 Mr Wells confirmed the parenteral transmission of BSE to a pig.(YB90/7.20/2.1)
The pig was inoculated in February/March of 1989 and was slaughtered in July 1990.(S Wells 2nd para 40) An
interim report was prepared for SEAC(84) and a press conference was held on 24 September 1990
to announce the parenteral transmission of BSE to pigs.(85) The transmission of BSE to pigs was a
major factor in the ban on SBOs being extended to all animal feed. Experiments were also
conducted by orally dosing pigs with BSE infected material but when the pigs were killed after
seven years they were not found to be incubating the disease.(S Wells 2nd para 40 )

55.İİİİ By August 1990 a total of 10 cases of FSE in domestic cats had been confirmed.(S Wilesmith 2nd para 109 ) Mr
Wilesmith designed a questionnaire to be completed by the veterinarians who clinically identified
FSE for the purposes of an epidemiological investigation. In addition to this investigation, the
University of Bristol was subsequently granted a MAFF contract for a study in collaboration with
the NPU to ascertain whether the condition in cats was transmissible to mice and, if so, to
undertake strain typing of the agent.(S Wells 2nd para 104; YB 92/6.19/5.1 ) Mr Wells was appointed Project Officer to monitor the
study. When the study was completed it showed that the disease in cats was transmissible and
that similarities in the biological characteristics of FSE and BSE on transmission to mice indicated
that the two diseases probably arose from a common source.(J/VR/134/449 )

57.İİİİ On 17 September 1990 Mr Bradley circulated a minute with regards to an offer by Dr
Schellekers of the Netherlands to collaborate on attempting to transmit BSE to chimpanzees.(YB90/9.17/1.1)
Mr Wells and Dr Rosalind Ridley, who was conducting the marmoset experiment, told Mr Bradley
that they did not feel there was any greater justification for an attempted transmission in
chimpanzees than marmosets.(S Bradley 3rd para 40 ) Mr Bradley passed on this view to the CVO.(YB90/9.23/1.1; YB90/9.26/3.1 ). [This is ignorant beyond belief. Marmosets are New World monkeys only distantly related to great apes. -- webmaster]

64. In February 1991 Mr Mark Robinson began studies on the transmission of BSE to
mink.(S Wilesmith 2nd paras 117-118 ) This study was done in collaboration with the United States Department of Agriculture (USDA), the Agricultural Research Service (ARS), and the Department of Veterinary Science at the
University of Wisconsin, USA. The results of this study were discussed at the 10th CVL/NPU BSE
R&D meeting held on 27 April 1993.(YB93/4.27/1.1) The results indicated that mink were susceptible to BSE,
and in contrast to previous attempts to transmit scrapie to the species, were susceptible by the
oral route of challenge.(J/JVIR /75/2151)

67.İIn Spring 1991 Mr McGill performed a review of 200 brains that had, using the obex
histopathological method, been deemed BSE-negative.(110) This diagnostic approach, that had
been developed for use within the VIS, used a single section from the medulla to look for
spongiform change. In his review Mr McGill examined other parts of the brain.(111) In his statement
to the BSE Inquiry Mr McGill said:

Upon closer examination, three of the 200 'BSE-negative' brains proved positive for spongiform changes diagnostic of BSE.(112) This represents an overall diagnostic accuracy of 99.85%, exceeding the 99.6% previously published for the same standard diagnostic technique. Despite this, at the behest of MAFF managers, the emphasis of the study and its provisional title had to be changed, from accurately representing the whole negative 10%, to a study examining this 10% minus any mention whatsoever of BSE-affected cattle going undiagnosed. I therefore had to reluctantly locate and analyse three new BSE-negative suspect brains.(113)

76.İİİİ In mid-1991 it was decided that a proposed
survey of 300 deer brains would proceed.(124) As with
the hound survey, there were difficulties in collecting
the material in a manner optimal for histopathological
examinations.(See YB92/11.4/2.1) During the period 1986 to 1996,
26 deer brains were referred for examination to the
Consultant Pathology Unit at the CVL, but none of
these showed evidence of an SE.

99.İİİİ On 11 April 1992 Mr Bradley prepared a paper for the Lamming Expert Committee on
Animal Feedingstuffs.(153) Some of the areas covered in the paper were tallow, the danger of BSE
to pigs, the effect of the species barrier, tissue infectivity of lambs and calves, scrapie incidence
and the danger of dogs developing SEs.

103.İİİİ On 16 July 1992 a meeting was held at CVL
to discuss the research proposals relating to the
studies on SEs in a greater kudu at a zoo.(S Bradley 3rd para 65 ) Three
main experiments were proposed: to determine the
distribution of agent in tissues; to study the
epidemiology; and to strain type isolates from a brain
of a new case of spongiform encephalopathy. Formal
proposals were later drawn up and Mr Bradley became
the Project Officer for the experiments.

108.İİİİ Mr Bradley and Mr Dawson met staff at
London Zoo on 23 March 1993 to discuss tissue
selection for the proposed transmission studies on
BSE-infected kudu material.(166) The Zoo did not want
to keep the kudu, but moving them to the CVL was
ruled out because of inadequate facilities to care for
them. The investigations into the distribution of the SE
agent in various tissues began in June 1993.

116.İİİİ In July 1993 studies involving the oral exposure of pigs to scrapie were started the
CVL.(179) Such studies were recommended by the expert committee on feedingstuffs chaired by
Professor Lamming, because it was found that pigs had been orally exposed not only to BSE but
also to scrapie. The pigs were orally exposed to scrapie-infected brain material in November 1993
and while the experiment remains in progress, no pigs have been shown to have developed the
disease to date.

121.İİİİ On 9 October 1993 Mr Wilesmith and others
published a paper on the additional cases of TSE in the
herd of greater kudu at London Zoo.(S Wilesmith 2nd para 95 ) On the basis
of feeding histories, the authors concluded that
horizontal transmission had occurred. However,
subsequent investigations based at the zoo revealed
that the affected animals were most likely to have
been infected from the feedborne source.

123.İİİİ In December 1993 Dr Ken Charlton of the Animal Disease Research Institute, Nepean,
Ontario, Canada, visited the CVL bringing material from a suspect case of BSE in Canada. The CVL
confirmed that the case was a BSE case and reported it to the Canadian authorities.(189) in 1994.

143.İİİİ On 3 July 1994 Mr Bradley was informed
that two more kudu were to be culled.(S Bradley 3rd para 86) He visited
the London Zoo on 21 July 1994 to review the
progress of the studies on TSEs in zoo animals.
Necropsies were to be carried out on the kudu and
tissues collected for further transmission studies. At
this stage the mice that had been inoculated with kudu
tissues in August and September 1993 had not
succumbed to spongiform encephalopathy. The Zoo
authorities wanted to move the kudu because of the
possibility of bad publicity.(YB95/2.10/1.6) This was discussed at
a SEAC meeting on 2 February 1995. The meeting
agreed that the risk to Zoo visitors was minuscule or
non-existent. Mr Bradley's case control study
indicated that infected feed was the most probable
cause of the BAB kudu SE cases.

152.İİİİ On 13-16 February 1995 ...
...BSE to pigs - Further work to clarify the finding of non-specific vacuolation in
the brains of control pigs was needed.

...BSE to chickens - Sub-passage in chickens and mice of various tissues from
experimentally infected birds was needed to clarify the findings of neurological
signs without neuropathology in inoculated birds.

A week of monkey business at Marwell!

"Our close cousins in the animal kingdom are the focus of activities at Marwell this week. Enjoy some "Primate
Awareness" as Marwell puts the spotlight on monkeys - from tiny tamarins to the acrobatic gibbons and macaques.
Marwell has fifteen species of primate which include the smallest in the world - the pygmy marmoset....The park is a member of the Madagascan Fauna Group. The fossas enclosures are planned to be built this year as a continuation of the World of Lemurs, another society-funded project which was opened by HRH The Princess Royal in 1992."

Endangered Species Golden Lion Tamarins (Leontopithecus rosalia
rosalia) inhabit a small area of tropical rain forest in south-eastern Brazil.
They have been severely persecuted in the wild, where their total population
has dropped as low as 400 in the early 1970¼s. Through the Smithsonian
Institute at the national Zoological Park in Washington DC, the Golden Lion
Tamarins have been internationally managed in the world¼s zoos. The result has
been a signicant increase in the captive population, leading to a
reintroduction programmes for tamarins back into the wild, where they are now
fully protected. Marwell has had 27 successful births in the collection, with 5
being released back to the wild as part of this programme.

The Chester zoo features a new orangutan, Baby female Jambi born to Subis, father Pulu came
to Chester from Australia). Cotton-topped tamarin, black and white ruffed lemur, cheetah, chimpanze, bornean orangutan, sumatran orangutan co-operative re-introduction programmes completed, in progress or planned. One of the largest chimpanzee colonies in the world, with over 80 births. Also white lipped and cotton-topped tamarins.

A lion was euthanized this year at a Scottish zoo (reportedly the Edinburgh Zoo) with confirmed FSE. Golden headed lion tamarinss are held there, along with 12 chimps.

The Paignton zoo has research programs on orangutans and houses Bulu, a 37 year old female, the oldest captive bred orangutan in Britain plus an all male group of 4 gorillas. There also capuchin
monkeys, white-bellied spider monkeys [Ateles belzebuth], Papio hamadryas baboons, and golden lion tamarins.

Paignton Zoo has five orang utans: Bulu, a female aged 36 who was the first captive bred orang utan in Britain; Gambira, Bulu's daughter born in April 1997; Senja, a female aged 18; Chinta, Senja's daughter aged 6; and Nakal, the only male in the group, aged 8. The group are all part of the European Endangered species Programme (EEP). Bulu has produced 11 offspring during her lifetime and has now been retired from breeding. Nakal is in the priority list of males to be bred as part of the EEP, but as he is closely related to Senja and Chinta it will be necessary to bring in one or two unrelated females for him, whereas Senja and Chinta will probably move to other breeding groups in Europe.

GOLDEN LION TAMARIN - Leontipithecus rosalia

Red data book status: Critically Endangered

Golden lion tamarins are one of 4 species of lion tamarin. In the wild they are restricted to a small area of rainforest, approximately 900 sq. km., in south east Brazil very close to the crowded conurbation of Rio de Janeiro. Golden lion tamarins are now protected by both Brazilian and International law, however the forest reserves are vulnerable to urban spread and agricultural and forestry development.

In 1992 surveys estimated the number left in the wild at around 500 and the zoo population at. Golden lion tamarins breed well in captivity and without doubt zoos have saved the species from extinction. The studbook is held by the National Zoological Park, Washington, USA. Reintroductions to the wild following began in 1984 and have achieved some success. By 1992 more then 100 golden lion tamarins had been reintroduced into the wild.

Golden lion tamarins have been breeding successfully at Paignton Zoo for a number of years. They live as a family group with a monogamous breeding pair as the dominant unit. Peanut (female) and Johan (male) dominated the group for five years during which time Peanut produced 5 sets of twins. She has now been retired and put on contraceptives.

One of Peanut's offspring, Gemma, has been included in the reintroduction programme. She was paired with Romario, who was bred at Jersey Zoo, and together they were sent to Chicago to be prepared for life in Brazil. Gemma has now produced three sets of twins and the family is being trained for release as a group.

ALLEN'S SWAMP MONKEY - Allenopithecus nigroviridis

Red data book status: lower risk

Allen's swamp monkeys are found in the swamp forests of Western Zaire and Angola. They inhabit a few protected reserves. Little is known of their status in the wild, nor of their behaviour and ecology. Surveys are urgently required to establish more information. It is likely that numbers have drastically declined and that the species is seriously threatened. The major threats to Allen's swamp monkeys are deforestation, persecution as agricultural pests and hunting for meat.

The zoo population numbered 59 in 1992. In 1994 a studbook matched pair arrived at Paignton, from Bristol and Edinburgh Zoos.

Under-diagnosis of CWD in elk: 10/17 infected

The Center for Food Safety faxed in documents obtained under a Freedom of Information Act filing in the autumn of 1998.

The first item, project number 3625-32000-026-00D log number 95517, is from Randall Cutlip's group at ARS, USDA, Ames, Iowa and is dated 19 Jan 98. Janice Miller is given as the scientitst to contact, 515-239-8316 or fax -8458. It consists of a summary and abstract of a paper that had already received four levels of approval by the USDA hierarchy (but still lacked NPS ADA and OCI Directer signatures).

The paper has not appeared 16 months later, suggesting political interference at USDA -- it contains some very bad news indeed.

The authors report on testing a captive herd of 17 elk that had previously experienced cases of CWD. This is easily identifiable as the South Dakota index game farm herd based on a previously reported slaughtered herd.

Of the 17 animals, only 2 had developed clinical signs. These, plus 1 non-clinical animal were definitely diagnosed as positive by histopathology. However 10 elk in total (including these 3) were diagnosed by IHC, so 7 new ones were found. thus 59% of the herd tested positive. This strongly suggests lateral transmission in these captive elk. This is only marginally less alarming than what Noelle Bons found with primates, 18 of 18 preclinicals testing positive.

One can see from these results why so many governments choose clinical signs, then histopathology, to IHC as the prefered detection method: they can then downplay the scope of epidemics by using the least sensitive test (so as not to alarm themselves or the public).

Taken at face value, this result says only 20% of the disease incubators (1 in 5) will be found by looking only at clinical animals and only 30% (3 in 10) of the cases will be found using standard histopathology (only in 1 of 8 preclinical animals). The obex of the medulla oblongata was the most reliable tissue; on the Wyoming CWD video, one can see a technician removing this in minutes withouta cracking open the skull.

By inference, the CWD epidemic in Colorado and Wyoming hasperhaps been understated by these factors. Survey data could be readjusted using these numbers, provided they didn't report zero. The distribution of disease, especially in early stages, could be extremely understated. It is very likely that efficient lateral transmission has occurred in this elk herd.

The Colorado Dept of Wildlife has erred in saying that the elk epidemic is no longer an issue in 1999 and no more testing was needed. They need to go back and repeat every survey in both deer and elk using IHC on the obex of the medulla oblongata. In fact, every state and region declaring itself free of disease needs to go back and repeat everything with this far better diagnostic method. If the incidence in free-ranging deer was 6% in 1998, by what method was this determined and how high is it really by this new method?

This is also extremely bad news for game farms and for wildlife adjacent to these farms (which have already been confirmed infected across a fence line in South Dakota). It suggests that the disease passes efficiently from one elk to the next and that for every 2 recognizable animals there could be another 8 silently incubating the disease and capable of transmitting it. As these elk are unwittingly swapped from one game farm to the next, the disease spreads silently.

Exactly the same thing is happening in British zoos. Here the need for outbreeding of rare and endangered species requires frequent shipping of animals internationally to maintain a proper studbook. Kirkwood gave the warning numerous times beginning in 1995 in Vet Record papers but it had no effect on zoos and MAFF cut off his grants in 1995.

A lot of pre-clinical elk and deer presumbably have already been eaten. But there is no reason to continue with the exposure of still more people. The USDA has sat on this paper for 16 months and counting. Here they had a clearly superior diagnositic method -- IHC of the obex of the medulla oblongata -- but they weren't sharing it with states doing deer and elk surveys the old way. And public hunting policy was being based on those survey results.

It might be a good idea to begin a tonsil biopsy program on long-term hunters from the Ft. Collins area. Because the disease has only had a short time to incubate, it makes no sense to keep exposing people while waiting a decade for cases to show up. Hunters in NE Colorado should probably be excluded as blood donors because it is particularly through the oral route that the lymph system gets infected.

And how many of the 6,000 US cows examined for BSE were diagnosed by IHC, as opposed to less sensitive methods? Maybe this survey needs to be re-done as well.

Further details on CWD

" I would like to make the following clarification. The work was done last summer (1998), a manuscript was subsequently submitted through the ARS approval system, and final approval was recieved September 28, 1998. The paper was then submitted as a brief communication to Veterinary Record. The journal returned the manuscript in December with reviewer comments that included many helpful suggestions for improvement.

However, the major concern was that the work should have presented a more detailed description of the neuroanatomical PrPSc localizations. Unfortunately, we were not able to meet such a requirement because the brain samples that had been collected were not appropriate for such a study. In view of this situation, we decided to withdraw the paper from consideration by Veterinary Record and the senior author is now rewriting the paper for submission to a different journal.

With regard to specific information presented in the paper, it should be noted that the 17 animals examined were a selected group taken from a very large herd and the selection process was not intended to provide a valid assessment of overall CWD prevalence [yet 8 of 10 elk are specifically described as preclinical; they may be older animals or ones with trace-back to Colorado or an infected hered or co-pasturing with clinical animals -- webmaster]

I don't think people familiar with the TSE literature on PrP immunohistochemistry (IHC) will be at all surprised that we were able to detect positive brains in elk that had not yet developed clinical signs or lesions. This kind of observation was reported several years ago using laboratory animal models of scrapie. Furthermore, in our 1993 and 1994 papers on the use of IHC for scrapie diagnosis in sheep, we reported finding many IHC positive brains that had been designated as only suggestive or inconclusive for scrapie by histopathological criteria. Since that time the APHIS National Veterinary Services Laboratory has been using IHC for diagnosis of TSEs. According to Drs. Linda Detwiler and Al Jenny, all brains from sheep, goats, cattle, deer, and elk with neurological disease are examined histologically and by IHC. [This may be true for _federally_ examined animals. However, there is no real federal program for CWD and no requirement for reporting or use of IHC. Indeed, the horror here is that inexperienced individual state fish and game departments -- or worse, state ag depts as in Idaho -- have taken over testing and are reporting null results using inferior and undescribed methods. -- webmaster]

Brains from the *downer cow* surveillance program are also examined by both tests. APHIS, with the assistance of state animal health and wildlife officials, has tested over 2000 brain samples from free-ranging cervids in Nebraska, South Dakota, Kansas, Michigan, and New Jersey. All brains were negative for PrPSc by IHC [yet South Dakota has had large numbers of confirmed cases: who tested these? -- webmaster]. State diagnostic laboratories know about the availability of IHC testing at the NVSL and tissue samples from suspect cases are sent to that laboratory on a referral basis.

I hope that someone directly involved in the Colorado and Wyoming CWD surveillance programs will comment on their use of IHC. However, I can say that from conversations with Drs. Mike Miller, Terry Spraker, and Beth Williams, I know that IHC has been used routinely in the diagnostic laboratories of both states for several years so undoubtedly the 1998 prevalence report was based on that type of testing procedure." [Yes, but what about 1997 and earlier years? -- webmaster]

Comment (webmaster):

It will be a cold day in hell before the British Veterinary Association (owner of Vet Record) and the CVO allow publication of a paper showing large percentages of preclinical animals, such as your elk. We are 19 years into the epidemic and still waiting.

The British have fought testing of preclinical cows throughout the BSE epidemic [see Fleetwood's testimony], fought surveying of sheep for preclinical BSE [proxy group: Anderson], fought testing of preclinical humans by tonsil test [proxy groups Will, Anderson], fought testing and reporting of preclinical zoo primates [CVO Meldrin], attacked primate TSE work in France [proxy group Will], attempted to discredit Collinge, Bons, and Almond among many others, insisted on a bogus methodology in the study of BSE in dogs, sought to suppress publication of clinical cases in nyala and others, refusal to provide material to qualified investigators in white tiger, cutting off grants to Kirkwood etc, refused to set aside frozen random samples, refused to use the Prionics or Irish test, and on and on and on.

This is the linchpin of their entire strategy: don't allow anyone to study or publish any pre-clinical anything. How can the only 3 British primates with BSE happen to be the only 3 British primates ever tested abroad?

As for TSE standards at Vet Record, look at this published flatulence (just for starters):

"With regard to specific information presented in the paper, it should be noted that the 17 animals examined were a selected group taken from a very large herd and the selection process was not intended to provide a valid assessment of overall CWD prevalence

-- Yet 8 of 10 elk are specifically described in the abstract as preclinical. The elk in fact were selected as older animals, ones with a trace-back history to Colorado or a contaminated facility, or co-pasturing with a clinical elk. This herd has been described in print before so why all the secrecy? To repeat, your study strongly validates concerns about horizontal transmission in elk.

"I don't think people familiar with the TSE literature on PrP immunohistochemistry (IHC) will be at all surprised that we were able to detect positive brains in elk that had not yet developed clinical signs or lesions."

-- Nobody is more familiar with this literature than the webmaster. I was actually very surprised by your report and delays in its dissemination because many states and countries are basing public policy on inferior methods. As you note, IHC is done solely in 'safe' scrapie or rabid cattle contexts. How many non-rabid downer cows have been tested with IHC and when will this be published?

"According to Drs. Linda Detwiler and Al Jenny, all brains from sheep, goats, cattle, deer, and elk with neurological disease are examined histologically and by IHC."

-- This may be true for _federally_ examined animals. However, CWD is not a federal disease. There is no requirement for state reporting of CWD nor use of IHC. Indeed, the horror here is that individual state fish and game departments -- or worse, state ag depts as in Idaho -- have taken over CWD testing and are reporting null results possibly deliberately using inferior methods for the purpose of fostering elk tag sales and elk farming.

" APHIS, with the assistance of state animal health and wildlife officials, has tested over 2000 brain samples from free-ranging cervids in Nebraska, South Dakota, Kansas, Michigan, and New Jersey. All brains were negative for PrPSc by IHC. State diagnostic laboratories know about the availability of IHC testing at the NVSL and tissue samples from suspect cases are sent to that laboratory on a referral basis."

-- No such study has ever been published nor, according to Freedom of Information, even been prepared. Why don't you simply copy and paste a draft of this study and the rejected one to this website for comment? This certainly does not constitute prior publication and might help expedite peer review and improve the final article (as recommended by the editorial board of PNAS).

-- These 2000 are overwelmingly deer, not elk. Yet we are supposed to eat elk sausage based on this. The South Dakota state veterinarian is reporting large numbers of confirmed cases in elk, even across fence lines to wild deer: who tested these? Nebraska and Oklahoma also announced positive cases. Other states announcing testing results or reporting CWD include Colorado, Utah, Nevada, Wyoming, Montana, and Wisconsin. Vermont refused to test elk despite imports from Colorado and Wyoming.

"I know that IHC has been used routinely in the diagnostic laboratories of both states [Colorado and Wyoming] for several years so undoubtedly the 1998 prevalence report was based on that type of testing procedure."

-- What about 1997 and earlier years? Miller announced that Colorado was refusing to test elk any further (duh: 51% of his dept revenue comes from elk tags). In other words, we have no idea whether 6% in deer and 1% in elk is increasing or decreasing because methods that severely understate the extent of the disease were (deliberately?) used in prior years (and samples were no doubt heaved or if saved, not re-examined). As you say, Colorado and the others _should_ have been using IHC on the obex for years and years. Wyoming is better off to the extent that samples went to Laramie rather than Fish and Game.

-- As far as local Fish and Game deptartments shooting themselves in the foot goes, I see in-house reports as self-serving anecdotes. There must be non-conflicted outside testing with timely and full release of data. I think we need to send samples to Switzerland or Germany -- the USDA is basically our counterpart to MAFF (meat sales promotion and safety under one roof). APHIS as you know is primarily a predator-killing subsidy to the cattle and sheep industries.

-- Let's test that 12 year old cow they had in with the deer (90% mortality) and elk at Foothills Research Station with IHC. Are you willing to test if I arrange for a sample to be sent? (Or was it "inadverently" thrown out?)

-- Let's test some tonsils collected from exposed hunters in the Ft. Collins area with IHC, why wait like the British did for 10 victims to show up. Would you be willing to do this if I arranged for samples to be sent?

Scrapie brains fed to US cows

The same group reports on 21 Oct 98 under project number 3625-32000-025-00D on a project beginning on 1 Oct 95.

Groups of steers fed raw or rendered scrapie brain remined normal after 86 and 82 months, resp. Nine animals euthanized early because of other disease tested normal with IHC and light microscopy. This does not favor US scrapie being much of a threat to US cows though the authors note that there may be other scrapie strains out there. The same argument would say that Marsh's mink did not get sick from downer cows because the cows had earlier eaten scrapie sheep.

Rendering industry insiders say USDA did not quantify titer in the raw material or resulting MBM that was rendered.
Also, the material from scrapie positive farms was rendered in a batch cooker, supposedly processed under "typical" US rendering conditions when actually they cooked the stuff in for 3 to 4 hours at a decent temp... almost 300 F with a long retention time.

Also, 14 calves were inoculated intracerebrally with CWD deerto determine its transmissiblity to cattle. No date is given for the start of that experiment. There were no results to report by Oct 98.

Show me the obex of the medulla oblongata

Medulla Oblongata - The medulla oblongata functions primarily as a relay station for the crossing of motor tracts between the spinal cord and the brain. It also contains the respiratory, vasomotor and cardiac centers, as well as many mechanisms for controlling reflex activities such as coughing, gagging, swallowing and vomiting.

The myelencephalon (medulla oblongata) surrounds the caudal half of the 4th ventricle and a small rostral portion of the central canal just caudal to obex. In CBA plate 6, follow the 4th ventricle in sagittal section to the point where it becomes enclosed, forming the central canal. This point is called obex. Obex is located between cross-sectional plates 39 and 40.

On the ventrolateral surface of the rostral medulla identify the olive - a protuberance caused by an underlying group of cells. On the ventral surface of the medulla find the pyramids. The pyramids constitute a collection of axons from the cerebral cortex, of which a portion arise from the precentral gyrus. The rootlets of the hypoglossal nerve emerge between the olive and the pyramid. CN's IX, X, XI emerge just dorsal to the olive. The caudal end of the lumen of the fourth ventricle is the obex.

Zoo animals in the US -- what happens with the dead ones?

US rendering industry correspondence 24 Apr 99

Question: What are the regulations concerning disposal of zoo animals in the US and when did they come into play? Do rendering companies still accept zoo animals or when did they stop? Zoos in Britain and Europe may have many animals incubating BSE, if these are shipped to the US for breeding programs and later die, would they end up at a rendering plant and then in cattle feed?

Answer: "Most states have regulations regarding the "safe disposal" of animals. State regulations are the same for domestic production animals from farms as for wild animals from zoos or roadkill. Some state regulations (maybe even a USDA requirement) specify particular disposal methods for animals or herds/flocks with specific disease conditions such as TB, avian influenza, etc. Also many diagnostic labs incinerate animals entering their facility, but others send what they consider lower risk animals and tissues to non-captive renderers who had few controls in place prior to 1996/97.

Getting back to the state regulations on disposal of animals, burial, rendering and incineration are the approved methods. A few years ago NJ allowed landfill disposal because many of the renderers would not take deadstock sheep and goats off farms and they did not allow or desire farm burial. Some states have recently allowed composting of certain species. Poultry deadstock, sometimes spent laying hens and dead pigs are frequently composted in some areas. A few states allow composting of cattle. Ohio State is a big center for research in this area.

No government agency has any regulation prohibiting disposal of zoo animals (or pets) from being rendered. I am sure some non-captive renderers take anything they can get their hands on. (Remember the article about Valley Protein in Baltimore a few years ago... elephant from zoo, police horse, cats and dogs, etc.) But to be fair, some non-captive renderers will not knowingly accept pets, sheep and goats, exotic animals, deer, etc. -- they only service butcher shops, farms and small slaughter establishments. Some have excellent controls to ensure their sources, others have "raw material policies" but lack controls and verification.

Then there are the captive rendering facilities which are associated with USDA inspected establishments (eg slaughterhouses). A few of these facilities also take material from outside sources, but most have complete contol of their raw material. Some process all the material entering their plant, while others segregate specific material and divert it to a non-captive renderer. For instance, a few plants only process material from animals that have passed USDA ante mortem inspection. Several major pet food manufacturers will only buy rendered Beef Meal or Beef and Bone Meal from these facilities. EU directive 90/667 defines this material as "low risk" and allows the importation of it when manufactured into petfood. At least one beef packer in the US removes CNS material from their process. USDA is now providing for free incineration of cattle with CNS disorders. Many renderers are offering transport of these animals from farms or packers to incineration facilities.

The crackings fed to French primates implies that rendered meat products were included. Cracklings
in Europe refer to the cooked meat fraction produced during rendering. They were probably pelleted or otherwise formed products. Carnivores tend to be fed fresh or thawed meats which are supplimented with
vitamins and minerals, not plant proteins.

It is doubtful if any monkey chow was exported to North America because there was never an economic incentive to do so (same reason little to no UK beef was imported before the USDA banned it in 1989). Several US companies have reputable specialty feeds for zoo and exotic animals... such as Purina. The UK feed trade did export quite a bit of feed to Europe, Africa and possibly elsewhere. From what I understand merchants from The Netherlands and Belgium tended to buy and sell these type of feeds and commodities such as MBM and they frequently altered documents showing country of origin. Anything for a Gilder.

Question: Can BSE contaminated blood be legally exported to the US? I am >concerned about continuing widespread use of blood as a milk replacer >in calves.

Answer:
USDA: The short answer is no. No live bovine or bovine product (except hides & milk?) can be legally
imported into the US from the UK or any European country. [USDA action in 1990 for BSE+ countries, further expanded for all of Europe in 1996].

FDA: The FDA allows pharmaceuticals with compounds made from tallow derivatives (via fatty acid hydrolysis & saponification) from Europe into the US. Medicines containing European gelatin are not allowed into the US based on existing European controls (or lack thereof)."

In England,The Animal By-Products Order 1992, as amended, imposes the basic requirement that animal waste is disposed of by rendering or incineration. There are some
exemptions from this requirement for material used for scientific purposes; for feeding to certain animals (zoo, circus or fur animals, recognised packs of hounds
(eg hounds in hunt kennels), and maggots farmed for fishing bait); and for use in knackers¼ yards. Low risk material may also be used in the production of pet food or technical or pharmaceutical products. Material may be buried, or burnt other than in an incinerator, only in certain circumstances (see paragraph 6) or when the Minister has served a notice on the person in charge of the waste, eg for disease control purposes.

Fax numbers and questionaire for zoos

Here are some questions to ask of your favorite zoo:
-- origin and brand name of monkey chow fed to animals 1985-1999
-- number of primates imported from France and UK 1985-1999
-- number of primates displaying neurological symptoms 1985-1999
-- number of deaths in primates for any reason 1985-1999
-- number of primates autopsied for TSE by anti-prion IHC 1985-1999
-- number of brain samples retained from animals not autopsied 1985-1999
-- number of primates incinerated without autopsy or retained brain sample 1985-1999

Here, the term 'zoo' includes zoo, research center, breeding facility, circus, pharmaceutical firm, etc., anywhere where these animals might be kept.

Or you can ask every zoo in Europe to clean up its act with one broadcast fax:

Epidemiological observations on spongiform encephalopathies in captive wild animals in the British
Isles.

Veterinary Science Group, Institute of Zoology, London.
Since 1986, scrapie-like spongiform encephalopathy has been diagnosed in 19 captive wild animals of eight species at or from eight zoological collections in the British
Isles. The affected animals have comprised members of the family Bovidae: one nyala (Tragelaphus angasi), four eland (Taurotragus oryx), and six greater kudu
(Tragelaphus strepsiceros), one gemsbok (Oryx gazella), one Arabian oryx (Oryx leucoryx), and one scimitar-horned oryx (Oryx dammah), and members of the family
Felidae: four cheetah (Acinonyx jubatus) and one puma (Felis concolor). In addition, three cases of a spongiform encephalopathy of unknown aetiology have been reported
in ostriches (Struthio camellus) from two zoos in north west Germany. Three features suggest that some of these cases may have been caused by the agent of bovine
spongiform encephalopathy (BSE). First, they have been temporally and geographically coincident with the BSE epidemic. Secondly, in all the ungulates for which details
are available, it is possible that either the affected animal itself, or the herd into which it was born or moved, had been exposed to proprietary feeds containing
ruminant-derived protein or other potentially contaminated material, and all the carnivores had been fed parts of cattle carcases judged unfit for human consumption.
Thirdly, the pathological results of inoculating mice with a homogenate of fixed brain tissue from the nyala and from one greater kudu were similar to the results of
inoculating mice with BSE brain tissue.

Spongiform encephalopathy in a captive puma (Felis concolor).

A captive adult puma developed ataxia, a hypermetric gait and whole body tremor. The signs progressed over a period of six weeks. Histopathological examination following
euthanasia demonstrated spongiform encephalopathy, gliosis and mild non-suppurative meningoencephalitis. Immunostaining with a polyclonal antiserum revealed prion
protein (PrP) associated with these changes in sections of cervical spinal cord and medulla. This is the first confirmed case of a scrapie-like spongiform encephalopathy
described in a non-domestic cat in the United Kingdom.

Spongiform encephalopathy in an arabian oryx (Oryx
leucoryx) and a greater kudu.

Clinical, pathological and epidemiological details of scrapie-like encephalopathies are
described in an arabian oryx and a greater kudu. Clinical signs included ataxia and loss of
condition with a short, progressive clinical course (22 and three days, respectively).
Histopathological examination of the brains revealed spongiform encephalopathy
characteristic of that observed in scrapie and bovine spongiform encephalopathy (BSE). It
seems probable that these cases have a common aetiology with BSE. Scrapie-like spongiform
encephalopathies have now been described in five species of exotic artiodactyls in Britain
indicating a, hitherto inapparent, wider range of ruminant species as natural hosts for these
diseases.

A small herd of greater kudu, derived from three individuals, has been maintained at the
Zoological Society of London since 1970. Spongiform encephalopathy has been diagnosed in five
out of eight of the animals born in this herd since 1987. With the possible exception of the
first confirmed case, none of these is thought to have been exposed to feeds containing
ruminant-derived protein. The pattern of incidence suggests that greater kudu are very
susceptible to the disease and that natural lateral transmission may have occurred among
them.

Ultrastructural features of spongiform encephalopathy
transmitted to mice from three species of bovidae.

British jerk around US researchers

168.İİİİ On 14 November 1989 Dr Watson minuted Mr Keith Meldrum. Dr Watson noted that 'if
we accede to Prusiner's request I believe that USDA and John Bourne/Jim Hope should be
informed. If brain material is not provided by us I have no doubt that he will obtain it
elsewhere.'(226)

169.İİİİ On 19 December 1989 Dr Prusiner wrote to Mr Bradley commenting that as previously
discussed he would require five brains from BSE-affected animals. He stated that the experiments
would 'involve the inoculation of both mice and hamsters with BSE brain as well as an examination
of the histopathology using anti-prion protein antibodies.' He continued that he would also be
analysing the 'BSE brain for PrPSc by Western blotting techniques using antibodies raised in rabbits
or mice.'(227) He then outlined details to be followed when packing and transportation of the
brains.

170.İİİİ On 8 January 1990 Dr Fraser wrote to Mr Bradley. In relation to Dr Prusiner's request
for five brains he commented that "surely one brain would be sufficient" for the transmission
experiments. He went on to say that "you are providing Stan (Prusiner) with an enormous amount
of material, it can't be necessary or justified on such a scale."(228)

171.İİİİ Dr Fraser wrote to Dr Watson the following day, again expressing his concern at the
experiments to be carried out by Dr Prusiner. He stated that 'Stan (Prusiner) has no previous work
on primary transmission, all his work concerns established lab strains. It is difficult therefore to
see the purpose of doing BSE transmissions in isolation.'(229)

172.İİİİ On 9 January 1990 Mr Wells wrote to Dr Watson with respect to Dr Prusiner's request
for BSE material. Mr Wells noted that the degree of co-operation to be afforded to Dr Prusiner's
requests is excessive and inappropriate to the CVL's interests and resources.(230)

173.İİİİ Mr Bradley sent a minute to Dr Watson on 23 January 1990, with respect to Dr
Prusiner's request for BSE material. Amongst others things, he made the following points:

1) "Now that the USA have released an import licence for BSE material there is a
'competition' for it which now includes Marsh, Breeze and Prusiner. Prusiner was first in
the sense of giving precise details of what he wanted and arranging to get material sent.
However the mink study also requires material.

2) It has been agreed by you, CVL Expt Leaders and NPU that we can send material to
Prusiner. All the demands of NPU and yourself have been satisfied in writing. The CVO and
Dr Bostock agree we should deliver providing there is no conflict with what we currently
are doing or plan to do soon.

3) It is up to Dr Prusiner to indicate what he needs for his studies rather than us and this
he has done. I believe we should try to provide, in the first instance, one brain to the
standard requested and to deal with the rest when we can. It was always understood
that we would retain samples of each brain for diagnosis, transmission and such other
studies as we deem necessary to confirm any of his findings if that subsequently was
required. I informed all people that he was wishing to transmit to laboratory animals. In
any case fixed material would not prevent that possibility."(231)

174.İİİİ Mr Bradley suggested that they supply Dr Prusiner with the first brain quickly and exactly
according to his request, and explain to him that they were not able to deal with the request for
the other four brains as quickly.

175.İİİİ On 12 February 1990 Mr Bradley prepared a submission on the collection of BSE brains.
The paper was submitted to a number of people including Mr Meldrum, Dr Watson and Mr Wells. Mr
Bradley noted that he had informed Dr Prusiner that the CVL would be able to obtain one of the
brains shortly and would endeavour to obtain the other four from the Veterinary Investigation
Service (VIS). He also noted that 'this sort of work is time consuming and expensive but may be
justified on the basis of international co-operation. However we cannot bring ourselves (at CVL) or
the VIS to a standstill just to satisfy others.'(232) In a hand-written annotation to the document Mr
Wells remarked:

'Who the hell does Prusiner think he is - "demanding" the protocol to his requirements
and why waste more time being concerned about his demands. He is not one of our
priorities!'(233)

176.İİİİ Dr Prusiner was finally sent the first brain on 30 April 1990. The letter sent from Mr
Wells accompanying the brain also proposed someone from CVL visiting Dr Prusiner to provide
additional experience in a technical area.(234) The remaining brains were subsequently provided in
co-operation with the VIS.(235)

177.İİİİ In evidence to the BSE Inquiry Dr Prusiner did not think that having obtained the brains
earlier would have enabled him to make any earlier findings. He stated that:

" Would we have made a major contribution if we had gotten it in 1998? [sic. should be
1988] I am not sure. Would we have put more effort into this much more quickly? I am
not sure. Did we discover anything with these particular brains at that point in time,
meaning in 1989 through let us say 1991, that we should have discovered a year earlier?
I do not think so. But it sure would have been nice to get them more rapidly.
It was just frustrating to continue to jump hoops and push people to get these brains.
We ended up with 12 brains in the end, not three. And we did a series of studies which
resulted in a manuscript which you undoubtedly have on which Gerald Wells and Ray
Bradley and John Wilesmith's name appear in the Journal of Infectious Disease in 1991 or
1993. I think it is actually 1993 by the time we published it.(236)"

197.İİİİ Prior to 1991 a number of requests were made to the CVL for material for transmission
studies. The requests extended to scientists both in Europe and the USA and included: